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机构地区:[1]西安交通大学医学院第一附属医院呼吸科,西安710061 [2]西安交通大学医学院环境与疾病相关基因教育部重点实验室
出 处:《四川大学学报(医学版)》2006年第1期60-62,共3页Journal of Sichuan University(Medical Sciences)
基 金:国家自然科学基金(批准号30171190)资助
摘 要:目的探讨人参皂甙-RG3在抑制肿瘤新生血管生成过程中的作用,对人肺腺癌A549细胞的影响及其内源性分泌的血管内皮细胞生长因子(VEGF)的作用。方法培养人肺腺癌细胞株A549细胞,采用MTT法检测不同浓度RG3(10-4MOL/L,10-5MOL/L,10-6MOL/L)对人肺腺癌A549细胞增生的影响、流式细胞仪观察不同浓度RG3(3×10-7MOL/L、10-6MOL/L,3×10-6MOL/L)对A549细胞凋亡的影响、放射免疫分析法定量检测细胞培养液中加入不同浓度RG3(10-7MOL/L、10-6MOL/L、10-5MOL/L和10-4MOL/L)后内源性VEGF含量的变化。结果RG3对A549细胞的增生无明显抑制作用,3×10-6MOL/L RG3作用120H后A549细胞凋亡百分数为29.8%(P<0.05)。RG3浓度为10-5MOL/L和10-4MOL/L组的VEGF明显低于对照组(P<0.05),10-4MOL/L RG3组的VEGF低于10-7MOL/L和10-6MOL/L RG3组,作用72H的VEGF水平明显低于48H和24H组(P<0.05)。结论适当浓度的RG3作用一定时间后,可促使人肺腺癌A549细胞的凋亡,并可抑制肿瘤细胞内源性分泌的VEGF含量,RG3抑制肿瘤血管生成机制之一是通过影响细胞分泌上述因子而起作用的。Objective To assess the effect of 20(R)-Rg3 on the inhibition of angiogenesis of lung cancer and explore its role in the change of endogenous VEGF secreted by A549 tumor cells themselves. Methods A549 tumor cells were cultured with different concentrations of 20(R)-Rg3 (10^-7 mol/L, 10^-6 mol/L, 10^-5 mol/L and 10^-4 mol/L), the VEGF contents were detected by ELASA method after 24 h, 48 h and 72 h. Cellular proliferation was detected by MTT method, and apoptosis was detected with flow cytometry. Results It was found that Rg3 had no significant inhibitory effect on the proliferation of A549 cells. The apoptosis rate was 29.8% after the cells being interfered with Rg3 at 3×10^-6 mol/L for 120 h. The levels of VEGF in the groups of Rg3 at 10^-5 mol/L and 10^-4 mol/L were lower than that in the contrast group (P〈0. 05). The level of VEGF in the group of 10^-4 mol/L was lower than that in the group of 10^-7 mol/L and group of 10^-6 mol/L, and it was lower after 72 h of interference than that after 24 h and 48 h of interfernce. Conclusion With the action of 20 (R)-Rg3, the level of VEGF secreted by A549 tumor cells themselves declined; the apoptosis of A549 tumor cells increased, especially at higher concentration and longer action time of Rg3. This might be one of the antiangiogenesis mechanisms of 20(R)-Rg3.
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